Abstract
BackgroundInsulin resistance may be assessed as whole body or hepatic.ObjectiveTo study factors associated with both types of insulin resistance.MethodsCross-sectional study of 182 obese children. Somatometric measurements were registered, and the following three adiposity indexes were compared: BMI, waist-to-height ratio and visceral adiposity. Whole-body insulin resistance was evaluated using HOMA-IR, with 2.5 as the cut-off point. Hepatic insulin resistance was considered for IGFBP-1 level quartiles 1 to 3 (<6.67 ng/ml). We determined metabolite and hormone levels and performed a liver ultrasound.ResultsThe majority, 73.1%, of obese children had whole-body insulin resistance and hepatic insulin resistance, while 7% did not have either type. HOMA-IR was negatively associated with IGFBP-1 and positively associated with BMI, triglycerides, leptin and mother's BMI. Girls had increased HOMA-IR. IGFBP-1 was negatively associated with waist-to-height ratio, age, leptin, HOMA-IR and IGF-I. We did not find HOMA-IR or IGFBP-1 associated with fatty liver.ConclusionIn school-aged children, BMI is the best metric to predict whole-body insulin resistance, and waist-to-height ratio is the best predictor of hepatic insulin resistance, indicating that central obesity is important for hepatic insulin resistance. The reciprocal negative association of IGFBP-1 and HOMA-IR may represent a strong interaction of the physiological processes of both whole-body and hepatic insulin resistance.
Highlights
Insulin resistance (IR) is an important metabolic alteration that is frequently associated with obesity and appears to be the primary mediator of metabolic syndrome [1]
In school-aged children, Body mass index (BMI) is the best metric to predict whole-body insulin resistance, and waist-to-height ratio is the best predictor of hepatic insulin resistance, indicating that central obesity is important for hepatic insulin resistance
The reciprocal negative association of insulin-like growth factor binding protein-1 (IGFBP-1) and Homeostatic Model Assessment-IR (HOMA-IR) may represent a strong interaction of the physiological processes of both whole-body and hepatic insulin resistance
Summary
Insulin resistance (IR) is an important metabolic alteration that is frequently associated with obesity and appears to be the primary mediator of metabolic syndrome [1]. Counter-regulatory hormone alteration is another factor involved in IR; in rodents, glucagon suppresses hepatic glucose production through activity regulated at the mediobasal hypothalamus through the vagus nerve [4]. The following heterogeneous signaling pathways participate in this process: liver cytohesin is required for insulin signaling and its inhibition by SecinH3 [7]; activation of NOTCH receptors results in lipolysis [8] and hepatic glucose production [9]; the target of rapamycin complex (TORC2) pathway modulates glucose expenditure [10]; and sterol regulatory element-binding protein-1 (SREBP-1) mediates insulin’s effect on fatty acid synthesis [11]. Insulin resistance may be assessed as whole body or hepatic
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